9. Emod Flashcards
wt does the PR interval represent?
normal value?
wt does larger than normal indicate?
Conduction delay/atrial depolarization (time for stimulus to spread through atria and pass AV junction)
normal = <0.2 sec
>0.2 sec –> first degree heart block
wt does QRS represent?
wt phase of action potential?
ventricular depolarization
phase 0
wt is brugada syndrome?
defective Na channels in cardiac myocytes
wt pump is responsible for repolarization?
Na-K ATPase
function of Na/Ca exchanger?
bring in Ca during systole
remove Ca during diastole
role of L-type Ca channels?
T -type?
L = phase 2 T = phase 0
wt is responsible for refractory period of conduction?
inactivated Na channels
is sympathetic or parasympathetic more predominant in regulating resting HR?
para
wt happens with a myocyte is overleaded w Ca?
Ca is removed via NCX and results in premature depolarizations
wt is Mobitz type 1 conduction block?
progressive lengthening of PR interval resulting in dropped beat
wt is Mobitz type 2 conduction block?
dropped beats not preceded by increased PR interval
2 short term txs for AV block?
permanant solution?
Vagolytic agent (atropine) or catecholamine (isoproterenol
pacemaker
wt is PSVT?
3 acute tx?
2 chronic tx?
DOC?
paroxysmal supraventricular tachy
- rapid onset and termination tachy
acute - adenosine, CCB, digoxin
Chronic - 1a (quinidine) 3 (amiodarone)
DOC - amiodarone
wt causes delayed after-depolarizations?
tx?
Ca overload
Ca blockers (verapamil)
wt causes a fib?
2 components?
block w multiple reentry
reduced conduction velocity
reduced refractory period
most important predisposing factor to EAD?
tx?
polonged APD
isoproterenol
wt channel abnormalities causes long-QT syndrome?
K mutations
Na mutations
wt is the principal of the conduction velocity approach to tx reentry?
block fast Na channels –> makes it a bidirectional block
2 ways to increase tissue refractoriness to tx reentry?
block Na channels from reactivating (no QT)
block outwar rectifier K channels (long QT)
2 factors affecting # of availability of Na channels?
membrane potential
recovery time constant
MOA of class 1A anti-arrhythmics?
ECG effects?
3 drugs?
Na blockers –> dec automaticity/CV
K blockers –> prolong APD
widen QRS and QT
Quinidine
procainamide
disopyramide
MOA of class 1B AA?
effect on QT?
name 2?
binds inactive Na channels –> prolongs refractory
no effects on QT or QRS
lidocaine mexilitine
MOA of class 1C AAs?
effect on ECG?
AE?
name 2
long acting Na channel blockers –> decrease CV
widen QRS
unidirectional block
flecainide propafenone
MOA of beta blockers/class II?
effect of ECG?
name 2
dec node conduction –> prevent shortening of APD and refractory period
prolong QT
propranolol, esmolol
MOA of class III drugs?
effect on ECG?
AE?
name 3
inhibit K channels –> prolong APD
prolong QT and PR and QRS
torsade de pointe
amiodarone, sotolol, bretylium
2 side effects of amiodarone?
corneal microdeposits
pulmonary fibrosis
MOA of class IV drugs?
use?
B blockers
control rate involving AV node
Tx for sinus bradycardia?
pacemaker
2 tx for sinus tachycardia?
beta blockers or CCB
tx for a fib/flutter if pt is hemodynamically unstable?
transthoracic cardioversion
should you tx a fib/flutter w rhythm or rate control?
4 rate drugs?
DOC for rhythm?
rate is better
digoxin
b blockers
CCB
amiodarone
amiodarone
2 drugs to tx monomorphic V tach and flutter?
1a
III
another name for polymorphic VT?
cause?
DOC?
torsade de pointes
long QT and Ca currents (EADs)
magnesium
tx for V fib?
cardioversion
contraindication for amiodarone?
lung disease
tx of choice for arrhythmias?
DC cardioversion
pacemaker
defibrillator
